Rapid cerebral ischemic preconditioning in mice deficient in endothelial and neuronal nitric oxide synthases
Rapid cerebral ischemic preconditioning in mice deficient in endothelial and neuronal nitric oxide synthases
复制标题
DOI：
10.1161/01.str.0000066870.70976.57
复制
发表时间：
2003-05-01
期刊：
影响因子：
8.3
通讯作者：
Huang, PL
中科院分区：
文献类型：
--
作者：
Atochin, DN;Clark, J;Huang, PL
背景和目的--本研究的目的是利用神经元和内皮型一氧化氮合酶(nNOS和eNOS)基因敲除小鼠来验证一氧化氮在局灶性脑缺血动物模型中需要进行预适应的假设。方法-用氢清除法(绝对)和激光多普勒血流仪(相对)测量野生型、nNOS和eNOS基因敲除小鼠的脑血流量。用3次5分钟的短暂性大脑中动脉闭塞(MCAO)对小鼠进行预适应，并进行永久性MCAO。结果：虽然野生型小鼠对缺血预适应有保护作用，但eNOS和nNOS基因敲除小鼠都没有保护作用。激光多普勒测量显示，各组核心缺血区的相对血流量下降是相同的。结论eNOS和nNOS基因敲除小鼠对快速缺血预适应都没有保护作用，提示一氧化氮可能在保护的分子机制中发挥作用。
Background and Purpose-The purpose of this study was to test the hypothesis that nitric oxide is required for preconditioning in an intact animal model of focal ischemia using neuronal and endothelial nitric oxide synthase (nNOS and eNOS) knockout mice.Methods-Cerebral blood flow was measured in wild-type, nNOS knockout, and eNOS knockout mice by hydrogen clearance (absolute) and laser Doppler flowmetry (relative). Mice were preconditioned by three 5-minute episodes of transient middle cerebral artery occlusion (MCAO) and subjected to permanent MCAO. Neurological deficit and infarct size were determined 24 hours later.Results-Although wild-type mice showed protection from ischemic preconditioning, neither eNOS nor nNOS knockout mice showed protection. Laser Doppler measurements indicated that the relative blood flow decreases in core ischemic areas were the same in all groups.Conclusions-Neither eNOS nor nNOS knockout mice show protection from rapid ischemic preconditioning, suggesting that nitric oxide may play a role in the molecular mechanisms of protection.